Amiloride reduces stroke and renalinjury in stroke-prone hypertensive rats

Sepehrdad, Reza; Chander, Praveen N.; Oruene, Alafuro; Rosenfeld, Louis; Levine, Seymour; Stier, Charles T.

doi:10.1016/s0895-7061(03)00006-2

Cited by 30 publications

(10 citation statements)

References 22 publications

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“…Does this organ saving effect of amiloride depend on the antihypertensive effect? In previous animal studies where amiloride and salt were given to deoxycorticosterone acetate treated rats and stroke-prone spontaneously hypertensive rats, amiloride improved cardiac fibrosis and decreased urinary protein excretion despite the facts that it did not decrease BP, affect serum potassium levels, or urinary electrolytes [40,41]. Additionally, where amiloride was given to uninephrectomized aldosterone-salt treated rat, it lowered elevated BP and attenuated myocardical fibrosis not only in left but also in right ventricle.…”

Section: Discussionmentioning

confidence: 96%

Aberrant ENaC activation in Dahl salt-sensitive rats

Kakizoe

Kitamura²,

Ko³

et al. 2009

Journal of Hypertension

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Section: Discussionmentioning

confidence: 96%

Aberrant ENaC activation in Dahl salt-sensitive rats

Kakizoe

Kitamura²,

Ko³

et al. 2009

Journal of Hypertension

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“…Radiotelemetry probes (TA11PA-C40; Data Sciences International, St. Paul, MN) were implanted using sterile techniques in rats anesthetized with sodium pentobarbital (50 mg/kg, ip; Abbott Laboratories, North Chicago, IL) as previously described [26–28]. Briefly, a midline abdominal incision was made and the telemetry probe catheter was introduced retrogradely into the descending aorta through a puncture site which was then sealed with tissue adhesive (3M Vetbond 1469, 3M Animal Care Products, St. Paul, MN).…”

Section: Methodsmentioning

confidence: 99%

Kinetics and Persistence of Cardiovascular and Locomotor Effects of Immobilization Stress and Influence of ACTH Treatment

Sabban¹,

Schilt²,

Serova³

et al. 2008

Neuroendocrinology

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(13 IU/kg, s.c.) triggered a short-lived rise in MAP, and decreased HR. After six daily injections of ACTH and recovery time (8 days), rats were immobilized as above. The cardiovascular responses were similar during the IMO, but the ACTHpretreated group displayed differences following cessation of the IMO. In addition, IMO led to a large reduction of locomotor activity during the dark (normally active) phase to levels similar to the light phase. Following the IMOs, locomotor activity recovered more slowly in the ACTH-pretreated group. The study revealed that IMO-triggered cardiovascular and locomotor responses are evident after termination of the stress. In addition, prior exposure to ACTH delayed recovery in cardiovascular and locomotor functions following cessation of stress.

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“…Interestingly, a 1961 publication a trial comparing prednisolone, placebo and calcium aspirin, reported no deterioration in patients on aspirin, whereas there was clear clinical worsening in the other two groups . Moreover, antihypertensive drugs with a protective effect on cerebrovascular disease, such as amiloride , may exert a neuroprotective effect in progressive MS . Finally, biotin, an important cofactor for many mitochondrial enzymes that protects against hypoxia associated energy failure may reverse disability in progressive MS .…”

Section: Ms and Svd: Evidence For A Possible Interactionmentioning

confidence: 99%

Age‐related small vessel disease: a potential contributor to neurodegeneration in multiple sclerosis

et al. 2017

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Multiple sclerosis (MS) is a chronic inflammatory demyelinating disorder of the central nervous system wherein, after an initial phase of transient neurological defects, slow neurological deterioration due to progressive neuronal loss ensues. Age is a major determinant of MS progression onset and disability. Over the past years, several mechanisms have been proposed to explain the key drivers of neurodegeneration and disability accumulation in MS. However, the effect of commonly encountered age-related cerebral vessel disease, namely small vessel disease (SVD), has been largely neglected and constitutes the aim of this review. SVD shares some features with MS, that is, white matter demyelination and brain atrophy, and has been shown to contribute to the neuronal damage seen in vascular cognitive impairment. Several lines of evidence suggest that an interaction between MS and SVD may influence MS-related neurodegeneration. SVD may contribute to hypoperfusion, reduced vascular reactivity and tissue hypoxia, features seen in MS. Venule and endothelium abnormalities have been documented in MS but the role of arterioles and of other neurovascular unit structures, such as the pericyte, has not been explored. Vascular risk factors (VRF) have recently been associated with faster progression in MS, though the mechanisms are unclear since very few studies have addressed the impact of VRF and SVD on MS imaging and pathology outcomes. Therapeutic agents targeting the microvasculature and the neurovascular unit may impact both SVD and MS and may benefit patients with dual pathology.

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Amiloride reduces stroke and renalinjury in stroke-prone hypertensive rats

Abstract: These findings suggest that interference with sodium channel function, perhaps at sites other than the kidney epithelium, may play a role in protecting against the evolution of cerebral and renal vascular injury in saline-drinking SHRSP.

Cited by 30 publications

References 22 publications

Aberrant ENaC activation in Dahl salt-sensitive rats

Aberrant ENaC activation in Dahl salt-sensitive rats

Kinetics and Persistence of Cardiovascular and Locomotor Effects of Immobilization Stress and Influence of ACTH Treatment

Age‐related small vessel disease: a potential contributor to neurodegeneration in multiple sclerosis

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